General
Preferred name
METHOCARBAMOL
Synonyms
Metocarbamol ()
AHR 85 ()
Robaxin ()
Lumirelax ()
NSC-170960 ()
Robaxin-750 ()
Delaxin ()
Forbaxin ()
Miolaxin ()
Neuraxin ()
Methocarbamol-d5 ()
P&D ID
PD001863
CAS
532-03-6
3967-43-9
145308-03-8
1189699-70-4
Tags
natural product
drug
available
Approved by
FDA
First approval
1957
Drug Status
approved
vet_approved
Max Phase
Phase 4
Drug indication
Relaxant (skeletal muscle)
Probe control
Probe control not defined
Orthogonal probes
0
No orthogonal probes found
Similar probes
0
No structurally similar probes found
Structure
P&D probe-likeness score
Structure formats
[[ format ]]
[[ compound[format === 'MOL' ? 'molblock' : format.toLowerCase()] ]]
Description
(extracted from source data)
DESCRIPTION
Methocarbamol is the carbamate of , but the carbamate bond is not metabolically hydrolysed, so guaifenesin is not a metabolite of methocarbamol. Methocarbamol has reduced abuse potential compared to other carbamate drugs such as and its prodrug .
(GtoPdb)
ABSORPTION
The time to maximum concentration is 1.1 hours for both healthy patients and those on hemodialysis.[A636] The maximum plasma concentration is 21.3mg/L for healthy patients and 28.7mg/L in hemodialysis patients.[A636] The area under the curve for healthy patients is 52.5mg/L\*hr and 87.1mg/L*hr in hemodialysis patients.[A636] AUC% based on terminal elimination half life is 2% for healthy patients and 4% for hemodialysis patients.[A636]; ; Older studies report maximum plasma concentrations in 0.5 hours.[A178366]
HALF-LIFE
The elimination half life is 1.14 hours in healthy subjects and 1.24 hours in subjects with renal insufficiency.[A636] Older studies report half lives of 1.6-2.15 hours.[A178366]
TOXICITY
Overdose of methocarbamol may be associated with alcohol and other central nervous system depressants.[Label] Patients may experience nausea, drowsiness, blurred vision, hypotension, seizures, and coma.[Label] Treatment of overdose is generally through airway maintenance, monitoring urinary output, vital signs, and giving fluid intravenously if necessary.[Label]; ; The oral LD50 in rats is 3576.2mg/kg.[L6295]; ; The FDA has classified methocarbamol as pregnancy category C.[Label] Animal and human studies have not been performed to determine the risks to a fetus, however fetal and congenital abnormalities have been reported.[Label] Methocarbamol is excreted in the milk of dogs, however it is unknown if this is also the case for humans.[Label] Caution should be exercised when taking methocarbamol while breastfeeding.[Label]; ; Studies to assess the carcinogenicity, mutagenicity, or effects on fertility of methocarbamol have not been performed.[Label]
ROE
In humans the majority of the dose is eliminated in the urine.[A178366] In dogs, 88.85% of the dose is eliminated in urine and 2.14% in the feces.[A178366] In rats, 84.5-92.5% of the dose is eliminated in the urine and 0-13.3% is eliminated in the feces.[A178366]
INDICATION
Methocarbamol tablets and intramuscular injections are indicated in the United States as an adjunct to rest, physical therapy, and other measures for the relief of discomforts associated with acute, painful musculoskeletal conditions.[Label,L6268] Oral methocarbamol in America may be given up to 1500mg 4 times daily for 2-3 days.[A31312]; ; In Canada, methocarbamol containing oral formulations are sold over the counter for pain associated with muscle spasm.[L6295] However, if these combination formulations include codeine, they are prescription only.[L6295]
MOA
The mechanism of action of methocarbamol is thought to be dependant on its central nervous system depressant activity.[A31312] This action may be mediated through blocking spinal polysynaptic reflexes, decreasing nerve transmission in spinal and supraspinal polysynaptic pathways, and prolonging the refractory period of muscle cells.[A178426,A178411] Methocarbamol has been found to have no effect on contraction of muscle fibres, motor end plates, or nerve fibres.[L6268]
PHARMACODYNAMICS
Methacarbamol is a skeletal muscle relaxant with an unknown mechanism of action.[A178426] Methacarbamol has been shown to block spinal polysynaptic reflexes, decrease nerve transmission in spinal and supraspinal polysynaptic pathways, and prolong the refractory period of muscle cells.[A178426,A178411] Methocarbamol does not act as a local anesthetic upon injection.[A178411] In animal studies, methocarbamol also prevents convulsions after electric shock.[A178426]
METABOLISM
Methocarbamol is metabolized in the liver by demethylation to 3-(2-hydroxyphenoxy)-1,2-propanediol-1-carbamate or hydroxylation to 3-(4-hydroxy-2-methoxyphenoxy)-1,2-propanediol-1-carbamate.[A178366] Methocarbamol and its metabolites are conjugated through glucuronidation or sulfation.[A178366]
[[ p.pathway_name ]]
[[ compound.targets[tid].gene_name ]]
Compound Sets
20
ChEMBL Approved Drugs
ChEMBL Drugs
DrugBank
DrugBank Approved Drugs
DrugCentral
DrugCentral Approved Drugs
DrugMatrix
Enamine BioReference Compounds
EU-OPENSCREEN Bioactive Compound Library
Guide to Pharmacology
MedChem Express Bioactive Compound Library
NCATS Inxight Approved Drugs
NIH Clinical Collections (NCC)
NPC Screening Collection
Prestwick Chemical Library
ReFrame library
Selleckchem Bioactive Compound Library
TargetMol Bioactive Compound Library
The Spectrum Collection
[[ a.name ]]
[[ ligand_id ]]
free of charge
External IDs
39
Molecular Weight
241.1
Hydrogen Bond Acceptors
5
Hydrogen Bond Donors
2
Rotatable Bonds
6
Ring Count
1
Aromatic Ring Count
1
cLogP
0.53
TPSA
91.01
Fraction CSP3
0.36
Chiral centers
1.0
Largest ring
6.0
QED
0.76
Structural alerts
0
No structural alerts detected
Related compounds
Custom attributes
(extracted from source data)
Pathway
Metabolism
Membrane Transporter/Ion Channel
Target
CA1
Sodium Channel
Carbonic Anhydrase
Source data
